Mercury is a heavy metal associated with cardiovascular diseases. Studies have reported increased vascular reactivity without changes in systolic blood pressure (SBP) after chronic mercury chloride (HgCl₂) exposure, an inorganic form of the metal, in normotensive rats. However, we do not know whether individuals in the prehypertensive phase, such as young spontaneously hypertensive rats (SHRs), are susceptible to increased arterial blood pressure. We investigated whether chronic HgCl₂ exposure in young SHRs accelerates hypertension development by studying the vascular function of mesenteric resistance arteries (MRAs) and SBP in young SHRs during the prehypertensive phase. Four-week-old male SHRs were divided into two groups: the SHR control group (vehicle) and the SHR HgCl₂ group (4 weeks of exposure). The results showed that HgCl₂ treatment accelerated the development of hypertension; reduced vascular reactivity to phenylephrine in MRAs; increased nitric oxide (NO) generation; promoted vascular dysfunction by increasing the production of reactive oxygen species (ROS), such as hydrogen peroxide (H₂O₂); increased Gp91Phox protein levels and in situ levels of superoxide anion (O^·−₂); and reduced vasoconstrictor prostanoid production compared to vehicle treatment. Although HgCl₂ accelerated the development of hypertension, the HgCl₂-exposed animals also exhibited a vasoprotective mechanism to counterbalance the rapid increase in SBP by decreasing vascular reactivity through H₂O₂ and NO overproduction. Our results suggest that HgCl₂ exposure potentiates this vasoprotective mechanism against the early establishment of hypertension. Therefore, we are concluding that chronic exposure to HgCl₂ in prehypertensive animals could enhance the risk for cardiovascular diseases.

中文翻译：

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高血压前期SHR中的慢性汞暴露通过增加NO和H2O2的产生来加速高血压的发展并激活血管保护机制。

汞是与心血管疾病有关的重金属。研究表明，在血压正常的大鼠中，慢性氯化汞（HgCl ₂）（一种金属的无机形式）暴露后，血管反应性增加，而收缩压（SBP）没有变化。但是，我们不知道高血压前期的个体，例如年轻的自发性高血压大鼠（SHRs）是否易受动脉血压升高的影响。我们通过研究高血压前期年轻SHRs中的肠系膜阻力动脉（MRA）和SBP的血管功能，研究了年轻SHRs中慢性HgCl ₂暴露是否加速了高血压的发展。将四周大的男性SHR分为两组：SHR对照组（车辆）和SHR HgCl₂组（暴露4周）。结果表明，HgCl ₂处理促进了高血压的发展。在MRA中降低了对去氧肾上腺素的血管反应性；一氧化氮（NO）生成增加; 通过增加过氧化氢（H ₂ O ₂）等活性氧（ROS）的产生来促进血管功能障碍；Gp91Phox蛋白水平和超氧阴离子原位水平（O ^·− ₂）增加；与媒介物治疗相比，减少了血管收缩素类前列腺素的产生。尽管HgCl ₂加速了高血压的发展，但是HgCl ₂暴露的动物还表现出血管保护机制，通过通过H ₂ O ₂和NO过量产生降低血管反应性来抵消SBP的迅速增加。我们的研究结果表明，HgCl ₂暴露增强了针对高血压早期形成的这种血管保护机制。因此，我们得出结论，高血压前期动物长期接触HgCl ₂可能会增加心血管疾病的风险。